The role of insulin resistance in non-alcoholic fatty liver disease is suggested by laboratory
data (hyperinsulinemia and decreased sensitivity to endogenous and exogenous insulin).
The clinical association with features of the metabolic syndrome, particularly in the most
aggressive stages of the disease, further confirms a causative role. Fat accumulation in the
liver may stem either from genetic defects, primarily responsible for insulin resistance, or
excessive calorie intake and visceral obesity, and is mediated by adipocytokines (leptin …